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Human NFKB1 Protein expressed in Wheat germ - ABIN1312483
Park, Hong, Park, Yoon, Seo, Hyun, Han, Ham, Hwang, Hong: Anticancer effect of tectochrysin in colon cancer cell via suppression of NF-kappaB activity and enhancement of death receptor expression. in Molecular cancer 2015
High NF-kappa-B expression is associated with lung cancer.
Studies indicate that NF-kappa B (NF-kappaB) is of particular interest to the space environment, as it is associated with many of the spaceflight-related health consequences [review].
In summary, we demonstrate that ADAMTS18 (show ADAMTS18 Proteins) silencing in breast cancer is significantly correlated with promoter CpG methylation. ADAMTS18 (show ADAMTS18 Proteins) acts as an antagonist of AKT (show AKT1 Proteins) and NF-kappaB signaling, further suppressing EMT (show ITK Proteins) and metastasis of breast cancer cells.
novel EGFR (show EGFR Proteins)-NF-kappaB-FOXC1 (show FOXC1 Proteins) signaling axis that is critical for BLBC cell function
NF-kappaB was the transcription factor targeted by most genes, and it regulated the expression of KDM6B, HDAC2 (show HDAC2 Proteins), MYC (show MYC Proteins), HSP90AB1 (show HSP90AB1 Proteins), and PABPC1 (show PABPC1 Proteins).
the NFKB1 -94ins/del ATTG promoter polymorphism may have a role in cancer susceptibility [meta-analysis]
Results indicate the involvement of IKK (show CHUK Proteins) and NF-kappaB signaling in the maintenance of glioblastoma stem cell.
The NFKB1 ATTG2/ATTG2 and CYP19A1 (show CYP19A1 Proteins) del/del genotypes are significantly associated with melanoma.
Overall, these results suggest that p53 (show TP53 Proteins) is involved in improving insulin (show INS Proteins) sensitivity of hepatic cells via inhibition of mitogen-activated protein kinases (MAPKs) and NF-kappaB pathways.
Thus, hypoxia not only increases RAGE (show AGER Proteins) expression in THP (show UMOD Proteins)-1cells by promoting nuclear translocation of NF-kappa B and HIF1alpha (show HIF1A Proteins), but also regulates chemotaxis and pro-inflammatory cytokines release, which may be partially mediated through upregulation of RAGE (show AGER Proteins) expression.
These results indicated that docosahexaenoic acid may attenuate lipopolysaccharide-stimulated inflammatory response in bovine mammary epithelial cells by suppressing NF-kappaB activation through a mechanism partly dependent on PPARgamma (show PPARG Proteins) activation.
Taken together, Staphylococcus aureus induces TGF-beta1 (show TGFB1 Proteins) and bFGF (show FGF2 Proteins) expression through the activation of AP-1 (show JUN Proteins) and NF-kappaB in bovine mammary gland fibroblasts.
Data indicate the involvement of PKC-alpha (show PKCa Proteins) in proMMP-2 activation and inhibition of TIMP-2 (show TIMP2 Proteins) expression by NF-kappaB-MT1-MMP (show MMP14 Proteins)-dependent and -independent pathway.
MMP-1 (show MMP1 Proteins) promotes VEGFR2 (show KDR Proteins) expression and proliferation of endothelial cells through stimulation of PAR-1 (show F2R Proteins) and activation of NF-kappaB
dynamic compression stimulates cell proliferation and proteoglycan (show Vcan Proteins) synthesis in the presence of IL-1beta (show IL1B Proteins) and/or inhibitors of the MAPKs and NFkappaB and AP-1 (show JUN Proteins) signalling pathways
TRIM5alpha (show TRIM5 Proteins) represses HIV-1 LTR promoter activity by negatively regulating TAK1 (show NR2C2 Proteins)/TAB1 (show TAB1 Proteins)/TAB2 (show TAB2 Proteins)/TAB3 (show TAB3 Proteins)-complex-mediated NF-kappaB activation.
This study showed that porcine epidemic diarrhea virus inhibited NF-kappaB activity and nsp1 was a potent NF-kappaB antagonist for suppression of both interferon (show IFNA Proteins) and early production of pro-inflammatory cytokines.
inhibition of NF-kappaB increases autophagy via JNK (show MAPK8 Proteins) signaling, and promotes steroidogenesis in porcine granulosa cells
SIRT1 (show SIRT1 Proteins), p53 (show TP53 Proteins) and NF-kappaB are involved in the control of both the proliferation and the apoptosis of ovarian cells.
porcine CD74 (show CD74 Proteins) significantly enhanced the inflammatory response by regulating the NF-kappaB signalling pathway during PCV2 infection, which suggests that porcine CD74 (show CD74 Proteins) may be implicated in the pathogenesis of PCV2 infection.
These results suggest that trans-10, cis (show CISH Proteins)-12-conjugated linoleic acid can modulate TNF-alpha (show TNF Proteins) production and NF-kappa B expression by a PPARgamma (show PPARG Proteins)-dependent pathway in porcine peripheral blood mononuclear cells.
The results obtained in the present study demonstrate for the first time that S100A8 (show S100A8 Proteins) as well as MyD88 (show MYD88 Proteins) and NF-B are activated by T3 and that these molecules are directly involved in the thyroid hormone (show PTH Proteins)-induced cardiac hypertrophic response. These data suggest that one of the mechanisms underlying T3-dependent cardiac hypertrophy/failure may involve the activation of an inflammatory pathway.
Our data suggest that rCC16 suppresses LPS (show TLR4 Proteins)-mediated inflammatory mediator TNF-alpha (show TNF Proteins), IL-6 (show IL6 Proteins), and IL-8 (show IL8 Proteins) production by inactivating NF-kappaB and p38 MAPK (show MAPK14 Proteins) but not AP-1 (show JUN Proteins) in RAW264.7 cells.
Our data indicate for the first time that the inflammasome is involved in the inflammatory response and cell death in hypoxia-induced beta cells through the ROS (show ROS1 Proteins)-TXNIP (show TXNIP Proteins)-NLRP3 (show NLRP3 Proteins) axis in vitro. This provides new insight into the relationship between hypoxia and inflammation in T2D.
Chronic overnutrition and astrocytic IKKbeta (show IKBKB Proteins)/NF-kappaB upregulation similarly impaired astrocytic plasticity, leading to sustained shortening of high-order processes. In physiology, astrocytic IKKbeta (show IKBKB Proteins)/NF-kappaB upregulation resulted in early-onset effects, including glucose intolerance and blood pressure rise, and late-onset effects, including body weight and fat gain.
The in vitro study illustrated that the anti-inflammatory effects of RA-XII were partially reversed following Nrf2 (show NFE2L2 Proteins) and HO-1 (show HMOX1 Proteins) inhibition. Together, these findings strongly suggested that RA-XII is a potential agent against acute kidney injury.
A new mouse modelof CLL was created by crossing the Emicro-TCL1 (show TCL1A Proteins) mouse with the previously described p50 (show LSP1 Proteins) knockout mouse4 to study the role of p50 (show LSP1 Proteins) in CLL pathogenesis. The knockout animals had lower leukocyte counts and less disease burden than the wild type, implying a role for p50 (show LSP1 Proteins) in CLL.
Results suggest that insufficient hepatocyte growth factor activator inhibitor type 1 (HAI-1 (show SPINT1 Proteins)) function promotes intestinal carcinogenesis by activating nuclear factor-kappaB (NF-kappaB) signaling.
Studied role of nuclear factor (NF)-E2-related factor-2 (Nrf2 (show NFE2L2 Proteins)) and NF-kappaB in inflammation and apoptosis induced by intestinal ischemia-reperfusion (IIR) in mice; findings indicate a critical role in IIR for Nrf2 (show NFE2L2 Proteins), possibly thru inhibition of NF-kappaB pathway.
UVB-irradiated or aged mice skin revealed that mTORC2 (show CRTC2 Proteins) activity was significantly upregulated which in turn increased Akt (show AKT1 Proteins) activation and Akt (show AKT1 Proteins)-dependent IkappaB kinase alpha (show CHUK Proteins) (IKKalpha (show CHUK Proteins)) phosphorylation, and The increased mTORC2 (show CRTC2 Proteins) signaling pathway during skin aging were associated to NF-kappaB activation.
Study indicate an essential role of NF-kappaB in gonadal differentiation.
This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. Two transcript variants encoding different isoforms have been found for this gene.
DNA binding factor KBF1
, DNA-binding factor KBF1
, nuclear factor NF-kappa-B p105 subunit
, nuclear factor NF-kappa-B p50 subunit
, nuclear factor kappa-B DNA binding subunit
, nuclear factor of kappa light chain gene enhancer in B-cells 1, p105
, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1, p105
, NF-kB p50 subunit
, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)
, nuclear factor kappa-B, subunit 1
, nuclear factor of kappa light polypeptide enhancer in B-cells 1
, nuclear factor kappa-B 1
, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1
, nuclear factor NF-kappa-B p105 subunit-like
, NF kappaB1
, NF-kappa-B1 p84/NF-kappa-B1 p98
, NF-kappaB p50
, nuclear factor kappaB p50
, nuclear factor-kappaB p50
, p50 subunit of NF kappaB
, p50 subunit of NF-kappaB
, BICD-related protein 1
, NF-kB1 precursor protein
, bicaudal D-related protein 1
, coiled-coil domain-containing protein 64A